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Afterload refers to the resistance the ventricle encounters as it tries to eject blood. Afterload is only conceptual and cannot be directly measured.

Factors affecting afterload

Afterload is increased by:

  • An increase in ventricular volume
  • An increase in arterial vasomotor tone (arterial vascular resistance)
  • A decrease in ventricular wall thickness

Afterload is decreased by:

  • A decrease in ventricular volume
  • A decrease in arterial vasomotor tone (arterial vascular resistance)
  • An increase in ventricular wall thickness

Since arterial vasomotor tone is a strong component of afterload, blood pressure or arterial vascular resistance is frequently used as a surrogate for afterload, although a weak surrogate.

Recall factors determining blood pressure

BP = CO x Arterial resistance

Factors that influence systolic blood pressure:

  • Stroke Volume, Stiffness of the arterial tree, Arterial resistance

Factors that influence diastolic blood pressure:

  • Duration of diastole, Elasticity in the arterial tree, Semilunar valve insufficiency, Arterial resistance

What is pulse pressure?

Pulse pressure refers to the difference between systolic BP and diastolic BP, also known as pulse width.

This is the main contributor determining the strength of the palpable peripheral pulse.

What is perfusion pressure?

Systemic perfusion pressure = Mean systemic BP – central venous pressure (right atrial pressure)

Pulmonary perfusion pressure = Mean pulmonary artery BP – mean pulmonary venous pressure

Assessment of systemic BP on physical examination

BP cannot be directly assessed by physical examination. Palpation of the arterial pulse provides very indirect information as to BP but is usually inadequate.

Measures of afterload

As mentioned above, afterload cannot be directly measured. However systemic arterial resistance can be measured but not without some difficulty. BP is a common but imperfect surrogate used to assess afterload.

Effect of afterload on myocardial performance

The effect of an increase in afterload is dependant on the inherent strength of the heart.

For a normal heart:

  • Very short term increases in afterload actually increase cardiac output.
  • More sustained increases in afterload result in a mild reduction in cardiac performance.

For a mildly depressed heart:

  • A moderate reduction in cardiac performance occurs with an increase in afterload.

For a heart with a severe reduction in contractility:

  • A profound reduction in stroke volume occurs with an increase in afterload.

Factors determining arterial resistance

The factors that determine arterial resistance are explained in Poiseuille’s Law:

Flow in a vessel is directly related to:

  • Change in pressure across the vessel
  • The radius of the vessel raised to the 4th power

Flow in a vessel is inversely related to:

  • The length of the vessel
  • Viscosity of blood (which is related to the # of red cells and protein content of the blood).

Recall: Flow = Pressure/Resistance

Manifestations of abnormal afterload

If afterload is too high:

  • Any disorder that causes a reduction in cardiac output will be associated with a “compensatory” increase in arterial vasomotor tone (systemic vascular resistance). Thus all cases of heart failure are associated with an increase in afterload.

If afterload is too low:

  • Signs of a low BP may be observed

Thus low BP may be observed with both an increase and decrease in afterload.

Effects of the autonomic nervous system on afterload

An increase in sympathetic tone increases afterload by increasing arterial resistance and increasing cardiac output via an increase in HR, preload (due to vasoconstriction) and Frank Starling’s Law, and an increase in contractility. Reducing sympathetic tone will have the opposite effect.

An increase in vagal tone will generally have the same effect as a decrease in sympathetic tone. A decrease in vagal tone will generally have the same effect as an increase in sympathetic tone.